id paper:paper_18681883_v7_n3_p403_Deniselle
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spelling paper:paper_18681883_v7_n3_p403_Deniselle2023-06-08T16:29:52Z Experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation experimental autoimmune encephalomyelitis motoneuron degeneration neuroinflammation neuroprotection progesterone Wobbler mouse amyloid precursor protein cell nucleus receptor growth associated protein membrane receptor neurotrophin progesterone sex hormone amyotrophic lateral sclerosis axon clinical trial (topic) demyelination disease severity drug effect enzyme metabolism evidence based practice experimental autoimmune encephalomyelitis human long term care motoneuron motoneuron degeneration motoneuron degeneration motor neuron disease multicenter study (topic) multiple sclerosis muscle strength nerve cell degeneration nervous system inflammation neuroprotection neurotransmission nonhuman priority journal protein expression relapse Review survival rate Far beyond its role in reproduction., progesterone exerts neuroprotective., promyelinating, and anti-inflammatory effects in the nervous system. These effects are amplified under pathological conditions., implying that changes of the local environment sensitize nervous tissues to steroid therapy. The present survey covers our results of progesterone neu-roprotection in a motoneuron neurodegeneration model and a neuroinflammation model. In the degenerating spinal cord of the Wobbler mouse., progesterone reverses the impaired expression of neurotrophins., increases enzymes of neu-rotransmission and metabolism., prevents oxidative damage of motoneurons and their vacuolar degeneration (paraptosis), and attenuates the development of mitochondrial abnormalities. After long-term treatment., progesterone also increases muscle strength and the survival of Wobbler mice. Subsequently., this review describes the effects of progesterone in mice with induced experimental autoimmune encephalomyelitis (EAE), a commonly used model of multiple sclerosis. In EAE mice., progesterone attenuates the clinical severity., decreases demy-elination and neuronal dysfunction., increases axonal counts., reduces the formation of amyloid precursor protein profiles., and decreases the aberrant expression of growth-associated proteins. These actions of progesterone may be due to multiple mechanisms., considering that classic nuclear receptors., extranuclear receptors., and membrane receptors are all expressed in the spinal cord. Although many aspects of progesterone action in humans remain unsolved., data provided by experimental models makes getting to this objective closer than previously expected. © 2011, by Walter de Gruyter Berlin Boston. All rights reserved. 2011 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_18681883_v7_n3_p403_Deniselle http://hdl.handle.net/20.500.12110/paper_18681883_v7_n3_p403_Deniselle
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic experimental autoimmune encephalomyelitis
motoneuron degeneration
neuroinflammation
neuroprotection
progesterone
Wobbler mouse
amyloid precursor protein
cell nucleus receptor
growth associated protein
membrane receptor
neurotrophin
progesterone
sex hormone
amyotrophic lateral sclerosis
axon
clinical trial (topic)
demyelination
disease severity
drug effect
enzyme metabolism
evidence based practice
experimental autoimmune encephalomyelitis
human
long term care
motoneuron
motoneuron degeneration
motoneuron degeneration
motor neuron disease
multicenter study (topic)
multiple sclerosis
muscle strength
nerve cell degeneration
nervous system inflammation
neuroprotection
neurotransmission
nonhuman
priority journal
protein expression
relapse
Review
survival rate
spellingShingle experimental autoimmune encephalomyelitis
motoneuron degeneration
neuroinflammation
neuroprotection
progesterone
Wobbler mouse
amyloid precursor protein
cell nucleus receptor
growth associated protein
membrane receptor
neurotrophin
progesterone
sex hormone
amyotrophic lateral sclerosis
axon
clinical trial (topic)
demyelination
disease severity
drug effect
enzyme metabolism
evidence based practice
experimental autoimmune encephalomyelitis
human
long term care
motoneuron
motoneuron degeneration
motoneuron degeneration
motor neuron disease
multicenter study (topic)
multiple sclerosis
muscle strength
nerve cell degeneration
nervous system inflammation
neuroprotection
neurotransmission
nonhuman
priority journal
protein expression
relapse
Review
survival rate
Experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation
topic_facet experimental autoimmune encephalomyelitis
motoneuron degeneration
neuroinflammation
neuroprotection
progesterone
Wobbler mouse
amyloid precursor protein
cell nucleus receptor
growth associated protein
membrane receptor
neurotrophin
progesterone
sex hormone
amyotrophic lateral sclerosis
axon
clinical trial (topic)
demyelination
disease severity
drug effect
enzyme metabolism
evidence based practice
experimental autoimmune encephalomyelitis
human
long term care
motoneuron
motoneuron degeneration
motoneuron degeneration
motor neuron disease
multicenter study (topic)
multiple sclerosis
muscle strength
nerve cell degeneration
nervous system inflammation
neuroprotection
neurotransmission
nonhuman
priority journal
protein expression
relapse
Review
survival rate
description Far beyond its role in reproduction., progesterone exerts neuroprotective., promyelinating, and anti-inflammatory effects in the nervous system. These effects are amplified under pathological conditions., implying that changes of the local environment sensitize nervous tissues to steroid therapy. The present survey covers our results of progesterone neu-roprotection in a motoneuron neurodegeneration model and a neuroinflammation model. In the degenerating spinal cord of the Wobbler mouse., progesterone reverses the impaired expression of neurotrophins., increases enzymes of neu-rotransmission and metabolism., prevents oxidative damage of motoneurons and their vacuolar degeneration (paraptosis), and attenuates the development of mitochondrial abnormalities. After long-term treatment., progesterone also increases muscle strength and the survival of Wobbler mice. Subsequently., this review describes the effects of progesterone in mice with induced experimental autoimmune encephalomyelitis (EAE), a commonly used model of multiple sclerosis. In EAE mice., progesterone attenuates the clinical severity., decreases demy-elination and neuronal dysfunction., increases axonal counts., reduces the formation of amyloid precursor protein profiles., and decreases the aberrant expression of growth-associated proteins. These actions of progesterone may be due to multiple mechanisms., considering that classic nuclear receptors., extranuclear receptors., and membrane receptors are all expressed in the spinal cord. Although many aspects of progesterone action in humans remain unsolved., data provided by experimental models makes getting to this objective closer than previously expected. © 2011, by Walter de Gruyter Berlin Boston. All rights reserved.
title Experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation
title_short Experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation
title_full Experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation
title_fullStr Experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation
title_full_unstemmed Experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation
title_sort experimental and clinical evidence for the protective role of progesterone in motoneuron degeneration and neuroinflammation
publishDate 2011
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_18681883_v7_n3_p403_Deniselle
http://hdl.handle.net/20.500.12110/paper_18681883_v7_n3_p403_Deniselle
_version_ 1768546693872091136